Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical course and prognosis were studied in 116 patients with clinical signs of ischaemic heart disease when they were hospitalized in an institution in which selective coronary angiography was practiced along with the routine clinical examinations. Control examinations were conducted 2 years later. The dynamics of the clinical manifestations and the results of the disease were evaluated according to the following categories: improvement, stabilization, progressive course, death. All the examined patients were divided into 2 groups: 74 patients with atherosclerotic coronary heart disease proved at angiography, and 72 patients without angiographic signs of coronary pathology. The course of the disease was found to depend on the presence and severity of the atherosclerotic process in the coronary arteries. Essential hypertension aggravated the course and prognosis of the disease. The distinctness of the clinical manifestations of coronary insufficiency, the ischaemic changes in the ECG repolarization complex, the duration of the disease history, and the age of the patients tended to predispose the outcome of the atherosclerotic lesion of the heart. In the group of patients with clinical signs of ischaemic heart disease, but without angiographic changes in the coronaries the result was more favourable, than in those with coronary atherosclerosis. This group, however, included some patients with prognostically unfavourable myocarcial lesions of non-atherosclerotic genesis.
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PMID:[Course and outcome of ischemic heart disease in patients with angiographically confirmed coronary arteriosclerosis]. 97 77

In a study attempting to improve coronary risk status, serum cholesterol and triglyceride levels were measured before and during treatment of 74 patients with mild primary hypertension. In 35 patients there was a satisfactory reduction in elevated blood pressure levels with diet therapy alone. In the remaining 39 patients a diuretic drug was required in addition to the diet. Diet therapy alone was followed by a decrease of 11 mg/100 ml in mean serum cholesterol (p less than 0.01 versus pretreatment value) and no change in serum triglyceride. The sue of diuretics was accompanied by an average increase of 11 mg/100 ml in serum cholesterol and of 34 mg/100 ml in serum triglyceride (p less than 0.01 versus pretreatment level for both). In a subgroup of 21 patients with greatest elevations in lipid levels during the administration of diuretics, little improvement in coronary risk status occurred because the increase in serum cholesterol balanced the decrease in systolic blood pressure, according to Framingham risk tables. If the level of serum lipids is a factor in the pathogenesis of coronary atherosclerosis then the observed effect of diuretic drugs to elevate serum cholesterol and triglyceride levels may explain, in part, the continuing high rate of occurrence of myocardial infarction during the treatment of hypertension.
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PMID:Elevation of serum lipid levels during diuretic therapy of hypertension. 98 73

Autopsy studies of atherosclerosis of the aorta and the coronary arteries were carried out in 3134 subjects with essential hypertension. A comparison was made with low, average, and high atherosclerosis groups. Essential hypertension was found to accelerate the development of all types of aortic lesion, except fatty streak, as compared with the standardized average atherosclerosis group, and to accelerate the development of fibrous plaque but not complicated and calcified lesions as compared with the high atherosclerosis group. The extent of fibrous plaque in the coronary arteries was greater in the essential hypertension group than in the low and standardized average atherosclerosis groups but did not differ from that in the high atherosclerosis group. The extent of complicated and calcified lesions and the prevalence of coronary stenosis were higher in the high atherosclerosis group than in cases of hypertension. Geographical differences in atherosclerosis among hypertensives in different towns reflected the findings for the whole material. Symptomatic hypertension was found to accelerate aortic atherosclerosis at least to the same extent as essential hypertension. It was conductive to coronary atherosclerosis but not to the same extent as essential hypertension. Coronary stenosis and various manifestations of coronary heart disease were rare in symptomatic hypertension.
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PMID:Atherosclerosis and hypertension. 108 93

Animal experiments have shown that the administration of calcium antagonists can prevent or slow the progression of atherosclerosis by inhibiting calcium overload and interfering with lipid metabolism and deposition. These encouraging results have prompted clinical trials to evaluate the effects of calcium antagonists (dihydropyridines and diphenylalkylamines) on atherosclerotic plaque formation. In patients with coronary heart disease, several studies have already shown that calcium antagonists can have a positive effect on plaque evolution, while in hypertensive patients no such study has been published to date. The Verapamil in Hypertension Atherosclerosis Study is an ongoing multicentre randomised double-blind parallel group trial comparing the antihypertensive efficacy of verapamil SR 240 mg/day with that of chlorthalidone 25 mg/day in 1464 patients with essential hypertension aged 40 to 65 years. In a randomised subgroup of patients (n = 550), who will be followed up for 3 years, B-mode ultrasonography is being employed to evaluate the effects of the 2 drugs on carotid wall thickness and carotid plaque development. Ultrasonographic evaluations are performed at baseline, after 3 months, and 1, 2 and 3 years after a standardised protocol to determine intimal-medial thickness in 4 segments of the extracranial carotid tree. The most interesting result to date is the high incidence of carotid alterations, with plaques present in 35% and arterial wall thickening in 31.8% of the 311 asymptomatic hypertensive patients processed so far. A preliminary evaluation of the antihypertensive efficacy of the trial medications after 6 months of double-blind treatment indicates a 63.5% response rate to monotherapy and a 7.8% drop-out rate because of drug inefficacy or intolerance.
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PMID:Preliminary clinical experience with calcium antagonists in atherosclerosis. Verapamil in Hypertension Atherosclerosis Study Investigators. 128 76

This study was performed to assess the possible involvement of humoral immunity in essential hypertension, independently of the presence of atherosclerotic disease, which in turn may be associated with immunologic changes. Sixty-five patients without demonstrated atherosclerotic disease were selected according to clinical and arteriographic criteria, including 23 hypertensive subjects (all pharmacologically treated) and 42 controls. Mean ages (58.7 +/- 8.3(1 S.D.) years in the controls and 57.7 +/- 7.9 years in the hypertensive subjects) and sex distribution were similar in the 2 groups. Of the main risk factors, atherosclerosis, smoking, diabetes, total cholesterol and HDL-cholesterol were equivalent, while triglycerides were higher in the hypertensive subjects than in the controls (142.6 +/- 52.7 vs. 112.6 +/- 67.7 mg/dl; p = 0.0065). In these subjects' sera the immunoglobulins IgG, IgA and IgM, and the third and fourth complement components (C3 and C4) were measured. Of these variables, only C3 was higher in the hypertensive subjects than in the controls (124.3 +/- 29.3 vs. 107.8 +/- 18.4 mg/dl; p = 0.0183). Furthermore, C3 was significantly correlated with triglycerides (tau = 0.3613; p < 0.0001), but the association with hypertension was confirmed only for C3, and not for triglycerides, by multiple logistic regression (p = 0.0142). The increase in serum C3 suggests the possible implication of humoral immunity in the pathogenesis or progression of essential hypertension.
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PMID:[Association of serum C3 and essential hypertension]. 129 20

Because the cause of hypertension is reversible in only 5 percent of patients, extensive initial work-up should only be considered in selected cases. Secondary causes should be suspected in patients whose hypertension begins before age 30 or after age 50 and in patients whose hypertension suddenly worsens after a long period of good control, becomes severe or malignant, or remains refractory to maximal medical therapy. A sudden reduction in renal function in a hypertensive patient and the discovery of a unilateral small kidney may also raise suspicion of a secondary cause. Renovascular disease, one of the most common secondary causes of hypertension, is usually the result of atherosclerosis in older patients and the result of fibromuscular dysplasia in younger patients. Physical examination seldom contributes to the diagnosis. The classic upper abdominal or flank bruit occurs in only 30 to 50 percent of patients with renovascular disease, and is not uncommon in patients with essential hypertension. The gold standard for diagnosis of renovascular disease remains the arteriogram. Transluminal renal angioplasty may be performed during arteriography if a high-grade stenosis is identified. Other management options include medical therapy and surgical revascularization with grafts.
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PMID:Percutaneous angioplasty for renovascular hypertension due to fibromuscular dysplasia. 132 61

As many as 24 patients suffering from essential hypertension (EH) were examined. The patients were subjected to Holter ECG monitoring, echocardiography, coronary angiography, exercise scintigraphy of the myocardium with transesophageal pacing of the atria and the dipyridamole test. The patients manifested defects of thallium accumulation during exercise scintigraphy of the myocardium. They were transitory defects of accumulation with clearance impairment recorded in EH patients with atherosclerosis of the coronary arteries; transitory defects of accumulation without clearance impairment recorded in EH patients with the angiographically unchanged coronary arteries. In Holter ECG monitoring, the patients with a silent depression of the ST segment demonstrated transitory defects of thallium accumulation by the myocardium in all the cases during exercise scintigraphy of the myocardium.
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PMID:[Hypertension and "silent" myocardial ischemia. I. The results of stress scintigraphy of the myocardium in patients]. 144 Mar 20

The clinical linkage of hypertensive cardiovascular disease, left ventricular hypertrophy, and accelerated atherosclerosis with a spectrum of metabolic disturbances including peripheral insulin resistance, hyperinsulinemia, obesity, and frank non-insulin dependent diabetes mellitus, has been increasingly appreciated. However, the underlying biologic basis mediating this clinical association remains unclear. Nuclear magnetic resonance techniques have been used to measure various intracellular ion species in human erythrocytes and have found that common, shared intracellular abnormalities of cytosolic free calcium, free magnesium, and pH occur in each of these clinical syndromes. Specifically, essential hypertension is characterized by higher fasting free cytosolic calcium concentrations and reciprocally lower intracellular free magnesium and pH levels compared with those of normotensive control subjects. Furthermore, for all subjects, free calcium and free magnesium levels were closely related both to the left ventricular mass and to the degree of insulin resistance present. Moreover, these same intracellular ionic lesions were found in normotensive obese and/or non-insulin diabetic individuals. Last, evidence has recently been provided that the cardiovascular consequences of increased dietary sugar and salt intake may well be determined by their concurrent influence on cellular ion metabolism. These data led to a hypothesis for a central role for altered cellular ion homeostasis in mediating the clinical linkage of cardiovascular and metabolic disease. According to this ionic hypothesis, essential hypertension, non-insulin dependent diabetes, and their frequently associated features of obesity, left ventricular hypertrophy, and accelerated atherosclerosis all derive from and reflect different clinical manifestations of the same underlying cellular lesion, characterized at least in part by elevated cytosolic free calcium and suppressed free magnesium levels.
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PMID:Cellular ions in hypertension, insulin resistance, obesity, and diabetes: a unifying theme. 145 64

The author describes and classifies the most frequently occurring combinations of peptic ulcer and pathology of other organs and systems on the basis of examining more than 2,000 patients. Diseases and syndromes associated with peptic ulcer are distributed into 2 groups: within the gastrointestinal tract and outside it. The former ones include cardia insufficiency, deranged bowel function, rectal syndrome, diseases of the gallbladder, pathology of the liver and pancreas; among the latter ones are essential hypertension, atherosclerosis, coronary heart disease, chronic nonspecific pulmonary diseases, and diabetes mellitus. Different pathogenetic relations and clinical load are shown to exist between the underlying disease and concomitant illnesses. Evidence is provided for the concept of enlarged spasms (phenomenon of the spastic dominant) common to peptic ulcer. Efficient methods of the individualized treatment of patients with concomitant pathology are described.
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PMID:[Peptic ulcer combined with other pathology. The clinical manifestations, course and therapy]. 150 63

Hypertension is a risk factor for coronary atherosclerosis possibly via an adverse effect on the vascular endothelium. Endothelium-mediated relaxation is impaired in animal models of hypertension. However, the effects of hypertension on human coronary artery endothelial cell function are unknown. To test whether endothelium-mediated relaxation is impaired in the coronary arteries of patients with hypertension, we studied 14 patients with essential hypertension requiring therapy and 15 nonhypertensive control patients undergoing cardiac catheterization. All had angiographically normal, smooth-appearing coronary arteries. Patients were matched for age and other coronary atherosclerosis risk factors. To assess endothelial cell function, the endothelium-dependent vasodilator acetylcholine (ACh, 0.01, 0.1, and 1.0 microM) and the endothelium-independent vasodilator nitroglycerin (40 micrograms) were selectively infused into the left anterior descending or circumflex coronary artery. Diameter change (expressed as percent) was assessed using quantitative angiography. There was a marked vasoconstrictor response to serial doses of ACh in hypertensive patients (-7%, -21%, and -27%) compared with control patients (-4%, -5%, and -7%) (p less than 0.02). The vasodilator response to nitroglycerin was preserved in hypertensive patients (+29%) and control patients (+25%) (p = NS), suggesting that endothelial cell dysfunction accounted for the differences in response to ACh. Thus, patients with hypertension have an accentuated coronary vasoconstrictor response to ACh, suggesting that endothelium-mediated regulation of coronary vascular tone is impaired by essential hypertension. This may reflect more generalized coronary endothelial changes contributing to the pathogenesis of atherosclerosis as well as hypertension.
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PMID:Epicardial coronary artery responses to acetylcholine are impaired in hypertensive patients. 151 54


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